Hypertension Flashcards
Give some non-pharmacological risk factors that can avoid the need for drug treatment
o Optimum body weight (BMI 20-25 kg/m2)o Regular physical activity (>30 mins a day)o Moderation of alcohol and salt. (
Give the grades for classifying hypertension
Grade 1 = 140-159 and 90-99Grade 2 = 160-179 and 100-109Grade 3 = >180 and >110
Give the main classes of antihypertensives
ACE inhibitorsAngiotensin antagonistsRenin AntagonistsCa2+ channel blockersThiazidesBeat blockers
Give some ACEi examples
RamiprilLisinoprilCaptopril
Give the mechanism for ACEi
Antagonise angiotensin converting enzyme, which converts angiontensin 1 to angiotensin 2. Reduces AT2 and aldosterone levels.Causes vasodilation and decreased TPR. Reduces bradykinin breakdown
ADRs of ACEi
Dry coughAngiooedemaHypotensionRenal failureHyperkalaemia
Give some angiotensin receptor blockers
LosartanValsartan
Mechanism for angiotensin receptor blockers
Block angiotensin 2 receptors- angiotensin receptor 1Inhibits vasoconstriction and aldosterone secretion
ADRs for angiotensin receptor blockers
Hyperkalaemia Renal failure
Give an example of a thiazide diuretic
Bendroflumethazide
Mechanism for thiazide diuretics
Antagonises Na-Cl co-transported in DCTBlocks Na+ and H2O reabsorptionLowers blood volume and blood pressure
ADRs of thiazides
HypkalaemiaHyperuricaemiaImpaired glucose toleranceHyponatremia, hypermagnesemia, hypercalcaemiaMetabolic alkalosisCholesterol and triglycerides increase
Why do you get hypokalaemia with thiazides?
Increased Na+ is reaching the CD where more Na+ is being reabsorbed via ENAC channels. Na+ must then be pumped into the blood via a basolateral Na+/K+ exchanger, leading to more K+ being excreted.
Why do you get metabolic alkalosis with thiazide diuretics?
Increased delivery of K+ to CD to allow for uptake of Na+ means that H+ is taken up into cells, due to K+/H+ exchanges, therefore leading to metabolic alkalosis.
Give some beta blockers
PropanololAtenololBisoprololSotololMetoprolol
Mechanism for beta blockers
Antagonise B-1 receptors in the heart, decreasing chronotropy and inotropy. This causes a decrease in oxygen demand and in the cardiac output. Also inhibits renin release, by decreasing the sympathetic drive.
ADRs of beta blockers
BronchospasmFatigue and insomniaDizzinessCold extremitiesHypotensionBradycardia
Give sone drug interactions that occur with beta antagonists
Prevents salbutamol from workingVerapamil also has a negative inotropic action
What are the three types of calcium antagonists?
DihydropyridinePhenylalkylamineBenzothiazepine
Describe dihydropyridine
Nifedipine and amlodipine- are 90% protein bound- liver metabolism- good oral absorptionADRS:SNS activationOedemaFlushing, sweating
Describe phenylalkylamines
Verapamil- prevents Ca2+ transport across myocardial and vascular smooth muscle- class 4 anti-arrthymic agent- peripheral vasodilation and reduced cardiac preload ADRS:constipationBradycardiaWorsen heart failure due to negative inotrophy
Describe benzothiazepines
Diltiazem- prevents Ca2+ transport across myocardial and vascular smooth muscle- prolongs AP and refractory period- peripheral vasodilation and reduced cardiac preloadADRS:BradycardiaWorsen heart failure due to negative inotrophy
Give a direct renin antagonist
Aliskiren
Mechanism for renin antagonist
Prevents action fo renin converting angiontensinogen to angiotensin 1
